The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines Chronic Obstructive Pulmonary Disease as a preventable and treatable disease with some significant extrapulmonary effects. The pulmonary component is characterized by airflow limitation that is not fully reversible.
The airflow limitation in COPD is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases. Severe COPD leads to respiratory failure, hospitalization and eventually death from suffocation. (Visit www.goldcopd.org for further reading about COPD)
Previously, COPD definitions have included emphysema and chronic bronchitis under the classification of COPD and it was often confusing because most patients with COPD present with overlapping signs and symptoms of these two distinct disease processes.
COPD may include diseases that cause airflow obstruction (e.g., emphysema, chronic bronchitis) or a combination of these disorders. Other diseases such as bronchiectasis, and asthma were previously classified as types of COPD. However, asthma is now considered a separate disorder and is classified as an abnormal airway condition characterized primarily by reversible inflammation. COPD can coexist with asthma.
Both of these diseases have the same major symptoms; however, symptoms are generally more variable in asthma than in COPD.
People with COPD commonly become symptomatic during the middle adult years, and the incidence of COPD increases with age. Although certain aspects of lung function normally decrease with age (e.g., vital capacity and forced expiratory volume in 1 second, COPD accentuates and accelerates these physiologic changes.
Here is an example of a nursing care plan for COPD.
Nursing Care Plan for COPD | Nursing Priorities; Discharge Goals
Nursing Priorities |Nursing Care Plan for COPD
Maintain airway patency.
Assist with measures to facilitate gas exchange.
Enhance nutritional intake.
Prevent complications, slow progression of condition.
Provide information about disease process/prognosis and treatment regimen.
Discharge Goals|Nursing Care Plan for COPD
Ventilation/oxygenation adequate to meet self-care needs.
Nutritional intake meeting caloric needs.
Disease process/prognosis and therapeutic regimen understood.
Plan in place to meet needs after discharge.
Nursing Care Plan for COPD | Nursing Diagnosis for COPD
Nursing Care Plan for COPD | Nursing Diagnosis for COPD; Desired Outcomes
Nursing Diagnosis for COPD: Airway Clearance, ineffective
May be related to
Increased production of secretions; retained secretions; thick, viscous secretions
Possibly evidenced by
Statement of difficulty breathing
Changes in depth/rate of respirations, use of accessory muscles
Auscultate breath sounds. Note adventitious breath sounds, e.g., wheezes, crackles, rhonchi. Rationale: Some degree of bronchospasm is present with obstructions in airway and may/may not be manifested in adventitious breath sounds, e.g., scattered, moist crackles (bronchitis); faint sounds, with expiratory wheezes (emphysema); or absent breath sounds (severe asthma).
Assess/monitor respiratory rate. Note inspiratory/expiratory ratio. Rationale: Tachypnea is usually present to some degree and may be pronounced on admission or during stress/concurrent acute infectious process. Respirations may be shallow and rapid, with prolonged expiration in comparison to inspiration.
Note presence/degree of dyspnea, e.g., reports of “air hunger,” restlessness, anxiety, respiratory distress, use of accessory muscles. Use 0–10 scale or American Thoracic Society’s “Grade of Breathlessness Scale” to rate breathing difficulty. Ascertain precipitating factors when possible. Differentiate acute episode from exacerbation of chronic dyspnea. Rationale: Respiratory dysfunction is variable depending on the underlying process, e.g., infection, allergic reaction, and the stage of chronicity in a patient with established COPD. Note: Using a 0–10 scale to rate dyspnea aids in quantifying and tracking changes in respiratory distress. Rapid onset of acute dyspnea may reflect pulmonary embolus.
Nursing Interventions for COPD
Airway Management (NIC)
Nursing Interventions for COPD (Independent) – continuation | Nursing Care Plan for COPD
Assist patient to assume position of comfort, e.g., elevate head of bed, have patient lean on overbed table or sit on edge of bed. Rationale: Elevation of the head of the bed facilitates respiratory function by use of gravity; however, patient in severe distress will seek the position that most eases breathing. Supporting arms/legs with table, pillows, and so on helps reduce muscle fatigue and can aid chest expansion.
Keep environmental pollution to a minimum, e.g., dust, smoke, and feather pillows, according to individual situation. Rationale: Precipitators of allergic type of respiratory reactions that can trigger/exacerbate onset of acute episode.
Encourage/assist with abdominal or pursed-lip breathing exercises. Rationale: Provides patient with some means to cope with/control dyspnea and reduce air-trapping.
Observe characteristics of cough, e.g., persistent, hacking, moist. Assist with measures to improve effectiveness of cough effort. Rationale: Cough can be persistent but ineffective, especially if patient is elderly, acutely ill, or debilitated. Coughing is most effective in an upright or in a head-down position after chest percussion.
Increase fluid intake to 3000 mL/day within cardiac tolerance. Provide warm/tepid liquids. Recommend intake of fluids between, instead of during, meals. Rationale: Hydration helps decrease the viscosity of secretions, facilitating expectoration. Using warm liquids may decrease bronchospasm. Fluids during meals can increase gastric distension and pressure on the diaphragm.
Beta-agonists: epinephrine (Adrenalin, Vaponefrin), albuterol (Proventil, Ventolin), terbutaline (Brethine, salmeterol (Serevent);pirbuterol (Maxair); Rationale: Inhaled beta2-adrenergic agonists are first-line therapies for rapid symptomatic improvement in severe Brethaire), isoetharine (Bronkosol, Bronkometer), bronchoconstriction. These medications relax smooth muscles and reduce local congestion, reducing airway spasm, wheezing, and mucus production. Medications may be oral, injected, or inhaled. Serevent is longer acting and can be used in combination with short-acting agents as needed.
Bronchodilators: e.g., anticholinergic agents: Rationale: Inhaled anticholinergic agents are now considered the ipratropium (Atrovent); first-line drugs for patients with stable COPD because studies indicate they have a longer duration of action with less toxicity potential while still providing the effective relief of the beta-agonists.
Methylxanthine derivatives, e.g., aminophylline, oxtriphylline (Choledyl), theophylline (Bronkodyl, Theo-Dur, Elixophyllin, Slo-Bid, Slo-Phyllin; Rationale: Decreases mucosal edema and smooth muscle spasm (bronchospasm) by indirectly increasing cyclic adenosine monophosphate (AMP). May also reduce muscle fatigue/respiratory failure by increasing diaphragmatic contractility. Use of theophylline may be of little or no benefit in presence of adequate beta-agonist regimen; however, it may sustain bronchodilation because effect of beta-agonist diminishes between doses.
Leukotriene antagonists: zafirlukast (Accolate); zileuton (Zyflo); Rationale: Reduces leukotriene activity to limit inflammatory response. In mild to moderate asthma, reduces need for inhaled beta2-agonists and systemic corticosteroids. Not effective in acute exacerbations because there is no bronchodilator effect.
Antiinflammatories [may be oral, nasal spray, MDI or DPI ], e.g., beclomethasone (Vanceril, Beclovent), triamcinolone (Azmacort); fluticasone (Flovent); cromolyn (Intal); flunisolide (AeroBid); budesonide (Pulmicort); nedocromil (Tilade); Rationale: Decreases local airway inflammation and edema by inhibiting effects of histamine and other mediators.
Oral, IV, and inhaled steroids: methylprednisolone (Medrol), dexamethasone (Decadron); Rationale: May be used to prevent allergic reactions/inhibit release of histamine, reducing severity and frequency of airway spasm, respiratory inflammation, and dyspnea. Note: Inhaled corticosteroids may cause local immunosuppression resulting in oral candidiasis infection.
Antimicrobials; Rationale: Various antimicrobials may be indicated for control of respiratory infection/pneumonia. Note: Even in the absence of pneumonia, therapy may enhance airflow and improve outcome.
Analgesics, cough suppressants, or antitussives, e.g., codeine, dextromethorphan products (Benylin DM, Comtrex, Novahistine); Rationale: Persistent, exhausting cough may need to be suppressed to conserve energy and permit patient to rest.
Artificial surfactant, e.g., colfosceril palmitate (Exosurf). Rationale: Research suggests aerosol administration may enhance expectoration of sputum, improve pulmonary function, and reduce lung volumes (air-trapping).
Provide supplemental humidification, e.g., ultrasonic nebulizer, aerosol room humidifier. Rationale: Humidity helps reduce viscosity of secretions, facilitating expectoration, and may reduce/prevent formation of thick mucous plugs in bronchioles.
Nursing Interventions for COPD
Airway Management (NIC)
Nursing Interventions for COPD (Collaborative) – continuation | Nursing Care Plan for COPD
Assist with respiratory treatments, e.g., spirometry, chest physiotherapy. Rationale: Breathing exercises help enhance diffusion; aerosol/nebulizer medications can reduce bronchospasm and stimulate expectoration. Postural drainage and percussion enhance removal of excessive/sticky secretions and improve ventilation of bottom lung segments. Note: Chest physiotherapy may aggravate bronchospasms in asthmatics.
Monitor/graph serial ABGs, pulse oximetry, chest x-ray. Rationale: Establishes baseline for monitoring progression/regression of disease process and complications. Note: Pulse oximetry readings detect changes in saturation as they are happening, helping to identify trends before patient is symptomatic. However, studies have shown that the accuracy of pulse oximetry may be questioned if patient has severe peripheral vasoconstriction.